RESPIRATORY Last edited: 3/9/2024

1. ASTHMA
I. PATHOPHYSIOLOGY III. CLASSIC FINDINGS OF ASTHMA V. DIAGNOSTIC APPROACH TO ASTHMA
II. CAUSES OF ASTHMA EXACERBATIONS A. DYSPNEA A. WORKUP FOR DYSPNEA SUSPECTED TO BE SECONDARY TO ASTHMA
A. ALLERGENS B. WHEEZING B. ASSESS FOR THE PRESENCE OF AN OBSTRUCTIVE LUNG DISEASE LIKE ASTHMA
B. VIRAL URTI IV. COMPLICATIONS OF ASTHMA VI. TREATMENT OF ASTHMA
C. DRUGS A. RESPIRATORY FAILURE A. ASSESS THE SEVERITY OF ASTHMA TO GUIDE STEPWISE TREATMENT
D. EXERCISE IN COLD AIR B. PNEUMOTHORAX B. ALTERNATIVE ASTHMA THERAPY
C. MANAGEMENT OF ASTHMA EXACERBATION

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I. Pathophysiology
o ↑Eosinophils, ↑Histamines/Leukotrienes
within the bronchioles →
↑Bronchiole wall edema and
↑Bronchoconstriction →
Narrowing of the bronchioles →
↑Resistance to airflow exiting lungs →
Obstruction of outgoing airflow →
Air trapped in alveoli → Wall Edema Mucus Bronchospasm
Dynamic hyperinflation of lungs →
Difficulty with breathing (short
inspiration and prolonged expiration) Airway Obstruction

Expiration Worse Air Trapping

Hyperinflation

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 04:34
II. Causes of Asthma Exacerbations
A. Allergens (e.g. Pollen, dust, mold, pet dander) B. Viral URTI (e.g. Rhinovirus, influenza)
o Allergens → Activate Dendritic Cells → o Viruses → Activation of Dendritic cells →
Dendritic cells stimulate TH2 cells → Dendritic cells stimulate TH2 cells →
TH2 cells release of IL-4 and IL-5 → TH2 cells release IL-4 and IL-5 →
This leads to stimulation of Eosinophils in bronchioles and also Causes stimulation of Eosinophils in bronchioles and stimulates
stimulates mast cells to release Histamines and Leukotrienes in mast cells to release Histamines and Leukotrienes in
bronchioles → Bronchospasm and Bronchial Wall Edema bronchioles → Bronchospasm and Bronchial Wall Edema
 Assess for Atopic Triad:
• Allergic Rhinitis
• Atopic Dermatitis
• Allergic Asthma

Dendritic cell

Eosinophils

IL-4/IL-5 Airway
Obstruction
TH2
Histamines
Leukotrienes
IgE
Plasma cells
Mast cells

C. Drugs (e.g. Beta-Blockers, ACE-I, Aspirin)

o Beta-Blockers → Bind to β2-receptors on bronchioles → Allergies*
Block bronchodilation → ↑Bronchoconstriction beyond normal
o ACE-I → ↑The production of bradykinin in bronchioles →
↑Bronchoconstriction beyond normal
o Aspirin → ↓Cyclo-oxygenase (COX) enzyme activity → Atopic
Triad
↓Prostaglandin and Thromboxane A2 formation →
Results in the remaining precursors to be shunted into the
Leukotriene pathway → ↑Leukotriene levels → Aspirin
↑Bronchoconstriction beyond normal
Assess for Samter’s Triad:
o Worsening Nasal Polyps post-aspirin use
o Worsening Sinusitis post-aspirin use
Samter's
o Worsening Asthma post-aspirin use Triad

D. Exercise → Especially in Cold Air Beta Blockers

o Exercise and Cold Air → Dries out the airway and directly Viral URTI’s*
triggers ↑Bronchoconstriction beyond normal
Cold Air/Exercise
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 III. Classic Findings of Asthma
Asthmatic patients remain asymptomatic with intermittent
asthmatic attacks or exacerbations
Asthmatic patients usually present with:

A. Dyspnea
o This occurs due to an obstruction of outgoing airflow →
Air is trapped in the alveoli →
Dynamic hyperinflation of lungs →
Difficulty taking a deep breath

B. Wheezing
o This occurs due to narrowing of the bronchioles → History: Dyspnea
↑Resistance to airflow exiting lungs →
Obstruction of outgoing airflow → Physical: Wheezing, Hyper-resonance
Wheezing sound can be heard during auscultation

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 IV. Complications of Asthma
A. Respiratory Failure (e.g. Status Asthmaticus) 11:28

Pathophysiology:
o Asthma exacerbations triggered by allergens or viral URTI →
Lead to increased bronchiole wall edema and Wheezing Silent Chest
bronchoconstriction → Narrowing of bronchioles, increased
resistance to airflow during exhalation, and subsequent
I:E Ratio
obstruction of outgoing air → Consequently, air becomes
trapped in the alveoli, causing dynamic lung hyperinflation →
This impedes the ability to inhale deeply and leads to alveolar
hypoventilation → There is a marked reduction in CO2
clearance and a slight impairment in O2 diffusion. In severe Hyperinflation
cases, this can progress to markedly elevated pCO2 and Pulsus Paradoxus
decreased paO2 → Resulting in Hypercapnic and Hypoxic
Respiratory Failure Hypoventilation
Presentation:
o Worsening dyspnea
o Tachypnea and ↑Work of breathing (WOB)
o Severe wheezing or silent chest (suggests no air movement)
o Pulsus Paradoxus:
 In patients with an asthma exacerbation, hyperinflation of
the lungs leads to a significant decrease in intrathoracic
pressure during inspiration → This increased negative
pressure allows a greater volume of blood to enter the RV
during ventricular filling → This results in a right-to-left shift
of the septum, causing it to bow into the LV, which
compromises LV filling → Consequently, there is a noticeable
decrease in SBP during inspiration, characterized by a drop Type II Respiratory
of > 10 mmHg in SBP Failure
ABG to Reveal Variable Findings: ( CO2+ O2)
o Respiratory Alkalosis:
 This indicates a less severe asthma exacerbation, as RR WOB Respiratory
evidenced by effective CO2 clearance resulting in alkalosis → Acidosis
The alkalosis is due to tachypnea from dynamic (Severe)
hyperinflation, which enables the patient to expel excess
CO2
o Normal ABG:
 This indicates a moderate asthma exacerbation: CO2
clearance is compromised, despite the presence of
tachypnea, suggesting increased CO2 retention →
Consequently, there is a pseudonormal pH, resulting from
the patient’s increased respiratory effort to expel CO2 due to
dynamic hyperinflation, and the gradual increase in CO2
levels caused by airway obstruction and respiratory muscle
fatigue
o Respiratory Acidosis:
 This indicates a severe asthma exacerbation → Despite
tachypnea, the patient is not eliminating CO2 effectively. This
likely results in CO2 trapping, leading to a reduced pH due to
CO2 retention from airway obstruction and respiratory
muscle fatigue

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 B. Pneumothorax 1 20:28

Pathophysiology:
o Obstruction of the outflow of air leads to air becoming
trapped within the alveoli → Resulting in dynamic
hyperinflation of the lungs → The subsequent increase in
intrapulmonary pressure can trigger barotrauma, causing
alveolar rupture → Air then leaks into the pleural cavity, raising
intrapleural pressure and compressing the lung
 Alveolar rupture often results from multiple factors →
During an asthma exacerbation, the need for mechanical
ventilation can lead to abnormally high airway pressures →
This, in turn, may cause barotrauma that leads to the
rupture of the alveoli
Presentation:
o Pleuritic Chest pain
o ↓Tactile fremitus
Hyperinflation
o Hyper-resonance to percussion
o Absent or ↓Breath sounds on the affected side

2 Pneumothorax

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 22:29
V. Diagnostic Approach to Asthma

A. Workup for Dyspnea suspected to be secondary to Asthma

1. Obtain CXR 3. Obtain ABG
Indications: Indications:
o Rule out other pulmonary causes of dyspnea (e.g. PNA, o Respiratory failure
Pulmonary edema, Pleural effusions, Pneumothorax)  May help with differentiating a primary Type I (hypoxic) from
Findings Supportive of Asthma Exacerbation: Type 2 (hypercapnic) respiratory failure
o Asthma usually will present with a normal CXR o Determine the severity of asthma
 If severe exacerbation → Can lead to hyperinflation of the Findings Supportive of Asthma Exacerbation:
lungs causing hyperluncency and flattening of the diaphragm o Respiratory Alkalosis:
(not common)  This indicates a less severe asthma exacerbation, as
evidenced by the clearance of CO2 leading to alkalosis. The
2. Obtain 12 Lead ECG alkalosis arises from tachypnea, which is a result of dynamic
Indications: hyperinflation, allowing the patient to exhale more CO2 than
o Rule out cardiac causes of dyspnea (e.g. Acute Myocardial normal
Infarction) o Normal ABG:
Findings Supportive of Asthma Exacerbation:  This indicates a moderate asthma exacerbation. Although
o Asthma usually will present with a normal ECG CO2 is being eliminated, it is not as effective as it should be
 If severe exacerbation → Can lead to pulmonary HTN since the patient is tachypneic. They are likely retaining more
causing right heart strain which would be evident by: CO2 than usual, leading to a pseudonormal pH. This is due to
• Right axis deviation the patient's attempts to expel excess CO2 caused by
• RBBB dynamic hyperinflation, combined with a gradual increase in
CO2 retention from airway obstruction and muscle fatigue
o Respiratory Acidosis:
 This indicates a severe asthma exacerbation, a late-stage
finding characterized by the inadequate clearance of CO2
despite being tachypneic. The patient is likely retaining a
significant amount of CO2, leading to a decreased pH. This
acidosis is a consequence of CO2 retention caused by airway
obstruction and muscle fatigue

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 B. Assess for the presence of an Obstructive Lung Disease like Asthma
1. Obtain Pulmonary Function Tests (PFTs)
Parameters of PFTs:
o FEV1/FVC ratio
o FEV1 post Bronchodilator administration
o FEV1 Post Methacholine administration
o Diffusion limitation of carbon monoxide (DLCO)
o Peak Expiratory Flow Rate (PEFR)
Indications:
o Determine if the patient has an obstructive vs restrictive lung
disease
Findings Supportive of Asthma:
o Obstructive Lung Disease Pattern that is Reversible:
 FEV1/FVC ratio < 70% suggests obstructive lung disease
• FEV1 helps to determine the severity of asthma
o ↓↓↓FEV1 → Suggests ↑↑↑the severity of asthma
 ↑↑ in FEV1 of > 12% from baseline after bronchodilator
Suggests a reversible obstructive lung disease like asthma
• Bronchodilators (e.g. albuterol) reduce resistance to
expiratory flow
 ↓↓in FEV1 of > 20% from baseline after Methacholine
Suggests an inducible obstructive lung disease like asthma
• Methacholine is a transient bronchoconstrictor that
increases resistance to expiratory flow
o This test is not commonly performed, but it may be
considered when the results from the FEV1/FVC ratio
and the FEV1 response to bronchodilators are
inconclusive, yet there is a strong suspicion of asthma
 DLCO is a less useful parameter as it can be normal or
increased
 PEFR is best utilized during asthma exacerbations to identify
the severity of an asthma exacerbation and monitor/trend
those values during treatment to assess for improvement or
deterioration
• PEFR < 40% predicted → Suggests a severe exacerbation
and should be admitted for close monitoring

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VI. Treatment of Asthma
A. Assess the Severity of Asthma to Guide Stepwise Treatment
Type of Asthma
Class Symptoms PFTs Exacerbations

< 2 daytime symptoms/wk

Intermittent FEV1 < 2/yr
< 2 nighttime symptoms/month
> 80%
(normal)
Mild Persistent

> 2 daytime symptoms/wk FEV1

Moderate Persistent > 2/yr
> 2 nighttime symptoms/month 60-80%

FEV1
Severe Persistent
< 60%

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1. Management of Intermittent Asthma 4. Management of Severe Persistent Asthma
Treatment: Treatment:
o Start Short-acting beta-2 agonist (SABA) → Albuterol PRN o Continue SABA PRN → Continue LABA
Purpose: o Increase Medium-dose ICS to High dose ICS
o SABA → Promotes bronchodilation → Improves expiratory  If poor response to low dose ICS → Up titrate to medium
airflow dose in moderate persistent asthma that is beginning to
Monitoring: bridge into severe persistent asthma
o Improvement in wheezing and dyspnea Purpose:
o SABA → Promotes bronchodilation → Improves expiratory
2. Management of Mild Persistent Asthma airflow
Treatment: o ICS → Promote reduction in airway inflammation → Reduces
o Continue SABA PRN bronchial edema and bronchoconstriction → Improves
o Add a low dose Inhaled corticosteroid (ICS) such as Budesonide expiratory airflow
daily o LABA → Promotes longer-acting bronchodilation → Improves
Purpose: expiratory airflow
o SABA → Promotes bronchodilation → Improves expiratory Monitoring:
airflow o Improvement in wheezing and dyspnea
o ICS → Promotes reduction in airway inflammation → Reduces  If no improvement escalate therapy given the patient is likely
bronchial edema and bronchoconstriction → Improves in the most severe form of persistent asthma:
expiratory airflow • Continue SABA PRN
Monitoring: • Continue LABA
o Improvement in wheezing and dyspnea • Continue High-dose ICS
3. Management of Moderate Persistent Asthma • Add Oral steroids and consider adding a Biologic such as
Omalizumab
Treatment:
o Continue SABA PRN
o Plus one of the two options:
 Add a Long-acting beta-2 agonist (LABA) daily such as
formoterol or Salmeterol and Continue the low-dose ICS daily
• This is the preferred regimen given the ease of escalating
the dose of the ICS if poor response
Purpose:
o SABA → promotes bronchodilation → improves expiratory
airflow
o ICS → Promotes reduction in airway inflammation → Reduces
bronchial edema and bronchoconstriction → Improves
expiratory airflow
o LABA → Promotes longer-acting bronchodilation → Improves
expiratory airflow
Monitoring:
o Improvement in wheezing and dyspnea
 If no improvement → Escalate therapy given the patient is
likely in between moderate and severe persistent asthma:
• Continue SABA PRN
• Continue LABA
• Increase Low-dose ICS to Medium-dose ICS

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 B. Alternative Asthma Therapy
1. Leukotriene Receptor Antagonists (LTRAs) 3. Mast Cell Stabilizers
(e.g. Montelukast) (e.g. Cromolyn sodium)
Indications: Indications:
o Allergic asthma o Allergic asthma
o Aspirin-induced asthma o Aspirin-induced asthma
Purpose: Purpose:
o Allergies and Asthma → ↑Leukotrienes o Prevents mast cell degranulation → Prevents release of
 LTRAs → ↓Leukotrienes → Reduces bronchial edema and histamine and leukotrienes → Reduces bronchial edema and
bronchoconstriction → Improves expiratory airflow bronchoconstriction → Improves expiratory airflow
Monitoring: Monitoring:
o Improvement in wheezing and dyspnea o Improvement in wheezing and dyspnea

2. Zileuton 4. Omalizumab
Indications: Indications:
o Prophylaxis for cold and exercise-induced asthma o Severe persistent asthma not responsive to LABA-ICS-SABA
Purpose: with ↑IgE and positive skin test for allergens
o Blocks the effects of leukotrienes → Reduces bronchial edema Purpose:
and bronchoconstriction → Improves expiratory airflow o This a monoclonal antibody that blocks the IgE antibody from
Monitoring: attaching to mast cells → Leads to a reduction in histamine and
o Improvement in wheezing and dyspnea leukotriene production → Reduces bronchial edema and
bronchoconstriction → Improves expiratory airflow
Monitoring:
o Improvement in wheezing and dyspnea
o Reduction in exacerbations/year providing sparing of steroid
use

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 C. Management of Asthma Exacerbation

1. Bronchodilators 3. Reduce Work of Breathing

Treatment: Treatment:
o Combination of SABA (e.g. albuterol) and SAMA (ipratropium) o Noninvasive Positive Pressure Ventilation (e.g. BIPAP)
 These are referred to as “Duonebs” and are often dosed  Given the discomfort of BIPAP, a patient is given Ketamine
every 6 hours which provides a dual function:
o Use of IV magnesium sulfate → One/two doses • Anxiolysis
Indications: • Bronchodilation
o First-line therapy in an asthma exacerbation o Invasive Positive Pressure Mechanical ventilation (e.g.
Purpose: intubation)
o To promote bronchodilation and assist in expiratory airflow Indications:
and resolution in air trapping o Severe tachypnea, wheezing or silent chest, and ↑WOB
Monitoring: o ↑↑PCO2 (Hypercapnia) → Suggests severe obstruction and
o Improvement in wheezing, dyspnea, RR and WOB poor CO2 clearance
o Improvement in PEFR from baseline/pretreatment  Hypercapnia can also lead to severe lethargy and sometimes
comatose states which can impair the protection of the
2. Reduce Airway Inflammation
airway
Treatment: Purpose:
o Systemic Corticosteroids: o Positive Pressure ventilation (e.g. BiPAP or intubation) →
 If able to swallow pills use Oral Prednisone usually 40-60mg Maintains bronchioles open due to higher airway pressure
(depending on severity) daily x 5-7 days delivery → Allows air to escape the lungs more easily →
 If unable to swallow pills given respiratory distress use IV Enables the lungs to deflate properly → Makes it easier for the
Methylprednisolone usually 40-125 mg (depending on patient to take a deep breath → Facilitates CO2 removal and
severity) every 6 hrs x 5-7 days results in improvement of tachypnea and WOB
Indications: Monitoring:
o Asthma exacerbation that is not improving with bronchodilator o Improvement in tachypnea, dyspnea, and WOB
therapy o Improvement in PCO2 on serial ABGs
Purpose: o Improvement in mental status if severely hypercapnic
Systemic Corticosteroids → Achieve higher than normal serum
steroid levels → Promote massive reduction in airway
inflammation → Massively reduces bronchial edema and
bronchoconstriction → Massively improves expiratory airflow
Monitoring:
o Improvement in wheezing, dyspnea, RR and WOB
o Improvement in PEFR from baseline/pre-treatment

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